The urinary bladder receives dual innervation from the autonomic nervous system. The sympathetic inhibitory fibers are believed to aid in urinary retention. Anything disrupting this pathway; such as anti-adrenergic drugs, may lead to urinary incontinence. However, urinary incontinence has not been reported with the clinical use of agents such as guanethidine, a powerful anti-adrenergic agent. One reason for the maintenance to bladder function may be the existence of a second inhibitory neurotransmitter to the bladder. ATP, or other purinergic compounds, have been shown to be effective inhibitors of urinary bladder function, which mimic the inhibitory effects of electrical stimulation of the sympathetic fibers to the bladder. In the present study, we are determining the physiological role of adenine analogs, specifically ATP, as possible inhibitors of bladder function. After using several techniques, including pretreatment with guanethidine or 6-hydroxydopamine or surgical sympathectomy, to disrupt the sympathetic innervation of the bladder, bladder function will be studied to determine if ATP is a physiological inhibitory transmitter in the bladder, and, if so, to determine the origin of the ATP. We will study the development of supersensitivity in the bladder to adrenergic or purinergic agents after disruption of the sympathetic pathway to the bladder.